Effect of diet-induced hypercholesterolemia on metabolic processes in the heart, liver, and pancreas in rats

Cover Page

Cite item

Full Text

Open Access Open Access
Restricted Access Access granted
Restricted Access Subscription or Fee Access


Aim. To analyze the biochemical changes in the cells of the heart muscle, liver and pancreas, as well as to establish their pathogenetic significance in diet-induced experimental hypercholesterolemia.

Methods. The study was conducted on 65 outbred male rats. During the experiment, the animals were divided into groups: the first (control, n=30) — animals that were kept on a general vivarium diet; the second (experimental, n=35) — animals with diet-induced hypercholesterolemia for three months by keeping on a special diet. At the end of the experiment, the concentrations of pyruvic acid, lactate, reduced glutathione, the activity of glutathione reductase, and glutathione peroxidase were determined in the tissues by using biochemical methods. The Student's t-test was used for the experimental data of the samples after normality testing.

Results. The analysis of energy metabolism indicators in animals with hypercholesterolemia relative to the control group revealed a lower level of pyruvic acid in the heart muscle (0.29±0.03 mmol/mg protein; p ≤0.05) and liver (0.25±0.02 mmol/mg protein; p >0.001). A significantly higher lactate level was recorded in all tissues, most pronounced in the liver (6.73±0.6 mmol/mg protein; p ≤0.001). The results obtained indicate the predominance of the anaerobic glycolysis in the tissues and the accumulation of incomplete-oxidation products. The study of the key glutathione-linked enzymes in animals with hypercholesterolemia relative to the control showed a lower activity of glutathione reductase in the pancreas — 0.52±0.05 mmol/mg protein/min (p ≤0.001), as well as its higher activity in the liver — 0.297±0.03 mmol/mg protein/min (p ≤0.001) and heart — 13.58±1.4 mmol/mg protein/min (p >0.001). The activity of glutathione peroxidase and reduced glutathione in all organs remained practically unchanged, or the differences were insignificant. This trend indicates a violation of the antioxidant defense system and oxidative stress.

Conclusion. Changes in the metabolic link of adaptive-compensatory responses in the cells of the heart muscle, liver, and, most pronounced in the pancreas, indicate the role of the pancreas as a “target organ” in the pathogenesis of diet-induced hypercholesterolemia.

Full Text

Restricted Access

About the authors

Z I Mikashinovich

Rostov State Medical University

Email: kbunpk-rostov@yandex.ru
SPIN-code: 5560-3924
Russian Federation, Rostov-on-Don, Russia

A V Romashenko

Rostov State Medical University

Email: romashenkoart@mail.ru
SPIN-code: 9368-8687
Russian Federation, Rostov-on-Don, Russia

I A Semenets

Rostov State Medical University

Author for correspondence.
Email: semenets.i.a@mail.ru
ORCID iD: 0000-0002-7945-7016
SPIN-code: 7985-4892
Russian Federation, Rostov-on-Don, Russia


  1. Akhmedzhanov N.M., Nebieridze D.V., Safaryan A.S., Vygodin V.A., Shuraev A.Yu., Tkacheva O.N., Lishuta A.S. Analysis of hypercholesterolemia prevalence in the outpatient practice (according to the ARGO study): part I. Rational Pharmacotherapy in Cardiology. 2015; 11 (3): 253–260. (In Russ.) doi: 10.20996/1819-6446-2015-11-3-253-260.
  2. Yachmeneva M.P., Ragino Yu.I. The role of hyperlipidemia and hyperglicemia in the development of coronary heart disease in young population. Ateroscleroz. 2018; 14 (1): 38–42. (In Russ.) doi: 10.15372/ATER­20180105.
  3. Karam I., Yang M., Li J. induce hyperlipidemia in rats using high fat diet investigating blood lipid and histopathology. J. Hematol. Blood Dis. 2018; 4 (1): 104. doi: 10.15744/2455-7641.4.104.
  4. Aronov D.M., Lupapov V.P. Athe­rosclerosis and coronary heart disease: some aspects of pathogenesis. Ateroskleroz i dislipidemii. 2011; (1): 48–56. (In Russ.)
  5. Babakova E.Yu., Trishina V.V., Tryasunova M.A. The relationship between biochemical chan­ges and the risk of ischemic stroke. Smolenskiy meditsinskiy al'manakh. 2015; (1): 58–59. (In Russ.)
  6. Gimaletdinova I.A., Amirov N.B., Absalyamova L.R. Liver, non-alcoholic fatty liver disease and dyslipidemia. Is there a connection? The Bulletin of Contemporary Clinical Medicine. 2020; 13 (6): 68–74. (In Russ.) doi: 10.20969/VSKM.2020.13(6).68-74.
  7. Tanaka Y., Ono M., Miyago M., Suzuki T., Miyazaki Y., Kawano M., Asahina M., Shirouchi B., Imaizumi K., Sato M. Low utilization of glucose in the liver causes ­diet-induced hypercholesterolemia in exogenously hypercholesterolemic rats. PLoS One. 2020; 15 (3): e0229669. doi: 10.1371/journal.pone.0229669.
  8. Otunola G.A., Oloyede O.B., Oladiji A.T., Afolayan A.J. Selected spices and their combination modulate hypercholesterolemia-induced oxidative stress in experimental rats. Biol. Res. 2014; 47: 5. doi: 10.1186/0717-6287-47-5.
  9. Serdyukov D.Y., Gordienko A.V., Saifullin R.F., Sapozhnikov T.V., Efimov O.I. Liver as target organ of the metabolic syndrome and lipid distress syndrome. Zdorov'e. Meditsinskaya ekologiya. Nauka. 2016; (4): 37–44. (In Russ.) doi: 10.18411/hmes.d-2016-152.
  10. Klyueva N.N., Okunevich I.V., Parfenova N.S., Belova E.V., Ageeva E.V. Effect of lipid-lowering activity of the natural original enzyme preparation in the experiment. Biomeditsinskaya khimiya. 2019; 65 (3): 227–230. (In Russ.) doi: 10.18097/PBMC20196503227.
  11. Nepomnyashchikh L.M., Lushnikova E.L., Polyakov E.L., Molodykh O.P., Klinnikova M.G., Russkikh G.S., Poteryaeva O.N., Nepomnyashchikh R.D., Pichigin V.I. Structural changes in the myocardium and serum lipid spectrum in experimental hypercholesterolemia and hypothyroidism. Bulletin of experimental biology and medicine. 2013; 155: 692–696. doi: 10.1007/s10517-013-2228-8.
  12. Mikashinovich Z.I., Belousova E.S., Semenets I.A., Romashenko A.V., Kantariya A.V. Modeling essential hypercholesterolemia. Patent for invention RF No. 2733693. Bulletin No. 28 issued at 16.03.2020. (In Russ.)
  13. Kalinina E.V., Chernov N.N., Aleid R., Novichkova M.D., Saprin A.N., Berezov T.T. Current views of antioxidative activity of glutathione and glutathione-depending enzymes. Vestnik Rossiyskoy akademii meditsinskikh nauk. 2010; (3): 46–54. (In Russ.)
  14. Spravochnik po kliniko-biokhimicheskom issledovaniyam i laboratornoy diagnostike. (Reference book on clnical and biochemical research and laboratory diagnostics.) Ed. by V.S. Kamyshnikova. M.: MEDpress-inform. 2009; 896 р. (In Russ.)
  15. Spravochnik po laboratornym metodam issledovaniy. (Laboratory research methods handbook.) Ed. by L.A. Danilovoy. SPb.: Piter. 2003; 736 р. (In Russ.)
  16. Ellman G.L. Tissue sulfhydryl groups. Arch. Biochem. Biophys. 1959; 82 (1): 70–77. doi: 10.1016/0003-9861(59)90090-6.
  17. Yusupova L.B. On increasing the accuracy of determining the activity of erythrocyte glutathione reductase. Laboratornoe delo. 1989; (4): 19–21. (In Russ.)
  18. Lowry O.H., Rosebrouph N.J., Farr A.L., Randall R.J. Protein measurement with the folin phenol reagent. J. Biol. Chem. 1951; 193 (1): 265–275. doi: 10.1016/S0021-9258(19)52451-6.
  19. Mel'nik A.A. The role of lactate in clinical practice. No­vosti meditsiny i farmatsii. 2019; (4): 686. (In Russ.)
  20. Ovchinnikov A.G., Arefieva T.I., Potekhina A.V., Filatova A.Yu., Ageev F.T., Boytsov S.A. The molecular and cellular mechanisms associated with a microvascular inflammation in the pathogenesis of heart failure with preserved ejection fraction. Acta Naturae. 2020; 12 (2): 40–51. doi: 10.32607/actanaturae.11154.
  21. Storozhuk P.G. Biokhimicheskaya priroda avtomatizma serdtsa, ego svyaz' s nervnoy sistemoy i ekstrapolya­tsiya khimicheskikh protsessov na elementy kardiogrammy. (The biochemical nature of the automatism of the heart, its connection with the nervous system and the extrapolation of chemical processes to the elements of the cardiogram.) Krasnodar: Izd-vo GBOU VPO KubGMU. 2011; 104 р. (In Russ.)

Supplementary files

There are no supplementary files to display.

© 2021 Eco-Vector

This website uses cookies

You consent to our cookies if you continue to use our website.

About Cookies